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Management of Spinal Tuberculosis in Young Children
Published in Alaaeldin (Alaa) Azmi Ahmad, Aakash Agarwal, Early-Onset Scoliosis, 2021
S. Rajasekaran, Sri Vijay Anand, Ajoy Prasad Shetty, Rishi Mugesh Kanna
GeneXpert is a cartridge-based nucleic-acid amplification (NAA) test. For osteoarticular tuberculosis, the pooled sensitivity and specificity of Xpert MTB/RIF (Mycobacterium tuberculosis/resistance to rifampin) were 96% and 85%, respectively, compared to culture tests [19]. It offers several advantages, such as shorter time for results (<2 hrs), portability and ability to use at remote locations, direct use without the need for processing, less contamination, and it poses less of a biohazard. The test also detects whether the organism is resistant to rifampicin by detection of defined mutations within the core region of the RNA polymerase b (rpoB) gene. In the era of drug-resistant tuberculosis, Xpert MTB/RIF assay is a vital tool and is recommended by the World Health Organization (WHO) for use worldwide. Commonly used diagnostic tests are summarised in Table 8g.1.
Role of Plant-Based Bioflavonoids in Combating Tuberculosis
Published in Megh R. Goyal, Durgesh Nandini Chauhan, Assessment of Medicinal Plants for Human Health, 2020
Alka Pawar, Yatendra Kumar Satija
Rifampicin (RIF) binds to beta RNA polymerase of bacteria and inhibits the RNA synthesis. It includes a set of antibacterial drugs and contains various derivatives viz., rifampicin, rifapentine, rifabutin, and rifalazil.3 Drug resistance is associated with mutation in 81bp region of rpoB gene, which encodes for beta RNA polymerase. INH and RIF with their derivatives are most common used drugs used for TB chemotherapy in combination with additional molecules.
Clinical Pharmacology of the Anti-Tuberculosis Drugs
Published in Lloyd N. Friedman, Martin Dedicoat, Peter D. O. Davies, Clinical Tuberculosis, 2020
Gerry Davies, Charles Peloquin
Rifampicin (RIF) is a semi-synthetic derivative of Rifamycin SV, a natural product of Amycolatopsis mediterranei. It is a moderately lipid-soluble and zwitterionic compound (log P 3.719, pKa 1.7/7.9, MW 822.94). RIF binds to the beta subunit of the mycobacterial DNA-dependent RNA polymerase enzyme, efficiently inhibiting transcription.32In vitro MIC99 for wild-type strains ranges from 0.03 to 0.5 μg/mL.3 The spontaneous rate of mutation conferring resistance is approximately 1 in 1010.4 Resistance is conferred by mutations clustered in an 81-bp region of the rpoB gene.5
Use of Xpert MTB/RIF and Xpert Ultra in extrapulmonary tuberculosis
Published in Expert Review of Anti-infective Therapy, 2021
Xpert MTB/RIF is a hemi-nested PCR that uses the GeneXpert platform for specimen preparation, amplification, and detection of the rifampicin resistance-determining region (RRDR) of MTB rpoB gene [12,13]. The system consists of an instrument, personal computer, barcode scanner, preloaded software, and single-use disposable cartridges. It uses a 6-colored laser-detection device (see Picture 1) [12]. Five rpoB RRDR-specific molecular beacons (nucleic acid probes) are used to detect either the presence or absence of the normal rifampicin-susceptible wild-type sequence of the rpoB gene and mutations which are responsible for 95% of the RR-TB cases. If a beacon binds to the matching sequence, it fluoresces suggesting the presence of a gene sequence that is characteristic of rifampicin-susceptible TB. If a beacon fails to bind to a matching sequence or if binding is delayed, this suggests potential resistance to rifampicin [13].
Antimicrobial resistance in Clostridium difficile ribotype 017
Published in Expert Review of Anti-infective Therapy, 2020
Korakrit Imwattana, Daniel R. Knight, Brian Kullin, Deirdre A. Collins, Papanin Putsathit, Pattarachai Kiratisin, Thomas V. Riley
Rifaximin is a derivative of rifampicin, an antimicrobial that inhibits RNA synthesis. Initially, it was proposed as adjunctive therapy for CDI due to its potent in vitro activity against C. difficile and low systemic absorption [86]. However, the prevalence of rifampicin and rifaximin resistance has gradually increased and resistance was associated with CDI outbreaks in the United States [17,87]. C. difficile RT 017 has been reported to have a higher prevalence of resistance to rifaximin than other common RTs in both Europe and Asia [29,51]. Missense mutations in the rpoB gene, which encodes a beta subunit of the RNA polymerase enzyme, reduce the affinity of the enzyme to both rifaximin and rifampicin and confer cross-resistance to the agents. Several amino acid substitutions in rpoB have been associated with rifaximin resistance in C. difficile [47]. A genomic study of C. difficile RT 017 documented R505K and H502N substitutions in a third of C. difficile RT 017 strains (32.5%; 90/277 and 33.2%; 92/277, respectively). Interestingly, one isolate in this study remained susceptible to rifampicin despite having both the R505K and H502N substitutions [88].
Helicobacter pylori: molecular basis for colonization and survival in gastric environment and resistance to antibiotics. A short review
Published in Infectious Diseases, 2019
Sharmila Fagoonee, Rinaldo Pellicano
In the last decade, rifabutin-based rescue therapies have offered a promising option after multiple H. pylori eradication failures. H. pylori has been shown to be highly susceptible in vitro to rifabutin, an antimycobacterial agent and a spiropiperidyl derivative of rifamycin S. Furthermore, selection of H. pylori resistant strains has been low under experimental conditions. Rifamycin targets the DNA-directed RNA polymerase and primarily the ß-subunit encoded by rpoB. Resistance to rifabutin is due to mutations at four distinct regions of this gene [56]. Recently, Hays et al. reported the molecular characterization of H. pylori resistance to rifabutin. By using rifampicin to screen for rifabutin resistance in vitro, the authors sequenced rpoB. All 54 resistant strains carried at least one mutation in rpoB at codons 525, 530, 538, 540 in the rifampicin resistance determining region. A new mutation, L547, responsible for rifamycins resistance was also reported [57].